期刊
ANTIOXIDANTS
卷 10, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/antiox10071117
关键词
pomegranate; mitochondrial DNA; DNA damage; apoptosis; oral cancer
资金
- Ministry of Science and Technology [MOST 108-2320-B-037-015-MY3]
- National Sun Yat-sen University-KMU Joint Research Project [NSYSUKMU 110-P016]
- Kaohsiung Medical University Hospital [KMUH109-9M56]
- Kaohsiung Medical University Research Center [KMU-TC108A04]
- NPUST-KMU joint research project [NPUST-KMU-110-P003]
Pomegranate polyphenolic extract POMx inhibits proliferation and induces apoptosis in oral cancer cells by impairing mitochondrial function.
The anticancer effect of pomegranate polyphenolic extract POMx in oral cancer cells has rarely been explored, especially where its impact on mitochondrial functioning is concerned. Here, we attempt to evaluate the proliferation modulating function and mechanism of POMx against human oral cancer (Ca9-22, HSC-3, and OC-2) cells. POMx induced ATP depletion, subG1 accumulation, and annexin V/Western blotting-detected apoptosis in these three oral cancer cell lines but showed no toxicity to normal oral cell lines (HGF-1). POMx triggered mitochondrial membrane potential (MitoMP) disruption and mitochondrial superoxide (MitoSOX) generation associated with the differential downregulation of several antioxidant gene mRNA/protein expressions in oral cancer cells. POMx downregulated mitochondrial mass, mitochondrial DNA copy number, and mitochondrial biogenesis gene mRNA/protein expression in oral cancer cells. Moreover, POMx induced both PCR-based mitochondrial DNA damage and gamma H2AX-detected nuclear DNA damage in oral cancer cells. In conclusion, POMx provides antiproliferation and apoptosis of oral cancer cells through mechanisms of mitochondrial impairment.
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